ArticleJournal of virology2013
Rotavirus-encoded nonstructural protein 1 modulates cellular apoptotic machinery by targeting tumor suppressor protein p53.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 48 citations in OpenAlex.
- Nuclear factor erythroid 2-related factor: potential use as a therapeutic strategy for viral infections.Archives of microbiology · 2026Review
- Understanding the mechanisms of mitochondrial rewiring during viral infections.The Journal of general virology · 2025Review
- Preclinical evaluation of oncolytic potential human rotavirus Wt 1-5 in gastric adenocarcinoma.PloS one · 2023Article
- Re-Examining Rotavirus Innate Immune Evasion: Potential Applications of the Reverse Genetics System.mBio · 2022Review
- Article
- Opposite Effects of Apoptotic and Necroptotic Cellular Pathways on Rotavirus Replication.Journal of virology · 2022Article
- Quercetin, a flavonoid, combats rotavirus infection by deactivating rotavirus-induced pro-survival NF-κB pathway.Frontiers in microbiology · 2022Article
- Adaptive homeostasis and the p53 isoform network.EMBO reports · 2021Review
- Treading a HOSTile path: Mapping the dynamic landscape of host cell-rotavirus interactions to explore novel host-directed curative dimensions.Virulence · 2021Review
- Viral Infection Modulates Mitochondrial Function.International journal of molecular sciences · 2021Review
- Rotavirus Interactions With Host Intestinal Epithelial Cells.Frontiers in immunology · 2021Review
- Rotavirus Induces Epithelial-Mesenchymal Transition Markers by Transcriptional Suppression of miRNA-29b.Frontiers in microbiology · 2021Article
- Progressive Rotavirus Infection Downregulates Redox-Sensitive Transcription Factor Nrf2 and Nrf2-Driven Transcription Units.Oxidative medicine and cellular longevity · 2020Article
- Biphasic regulation of RNA interference during rotavirus infection by modulation of Argonaute2.Cellular microbiology · 2019Article
- Activation of PI3K, Akt, and ERK during early rotavirus infection leads to V-ATPase-dependent endosomal acidification required for uncoating.PLoS pathogens · 2018Article
- Modulation of rotavirus severe gastroenteritis by the combination of probiotics and prebiotics.Archives of microbiology · 2017Review
- Effect of Leaf Surface Chemical Properties on Efficacy of Sanitizer for Rotavirus Inactivation.Applied and environmental microbiology · 2016Article
- Rotavirus NSP1 Associates with Components of the Cullin RING Ligase Family of E3 Ubiquitin Ligases.Journal of virology · 2016Article
- Review
- The BM2 protein of influenza B virus interacts with p53 and inhibits its transcriptional and apoptotic activities.Molecular and cellular biochemistry · 2015Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p53, a member of the innate immune system, is triggered under stress to induce cell growth arrest and apoptosis. Thus, p53 is an important target for viruses, as efficient infection depends on modulation of the host apoptotic machinery. This study focuses on how rotaviruses manipulate intricate p53 signaling for their advantage. Analysis of p53 expression revealed degradation of p53 during initial stages of rotavirus infection. However, in nonstructural protein-1 (NSP1) mutant strain A5-16, p53 degradation was not observed, suggesting a role of NSP1 in this process. This function of NSP1 was independent of its interferon or phosphatidylinositol 3-kinase (PI3K)/AKT modulation activity since p53 degradation was observed in Vero cells as well as in the presence of PI3K inhibitor. p53 transcript levels remained the same in SA11-infected cells (at 2 to 14 h postinfection), but p53 protein was stabilized only in the presence of MG132, suggesting a posttranslational process. NSP1 interacted with the DNA binding domain of p53, resulting in ubiquitination and proteasomal degradation of p53. Degradation of p53 during initial stages of infection inhibited apoptosis, as the proapoptotic genes PUMA and Bax were downregulated. During late viral infection, when progeny dissemination is the main objective, the NSP1-p53 interaction was diminished, resulting in restoration of the p53 level, with initiation of proapoptotic signaling ensuing. Overall results highlight the multiple strategies evolved by NSP1 to combat the host immune response.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.